Evidence map›Paper›PMID 34707383›Full record

ArticleJournal of inflammation research2021

Atherosclerosis Pathways are Activated in Pericoronary Adipose Tissue of Patients with Coronary Artery Disease.

Michał Konwerski, Agnieszka Gromadka, Adam Arendarczyk, Marta Koblowska, Roksana Iwanicka-Nowicka, Radosław Wilimski, Paweł Czub, Krzysztof Jerzy Filipiak, Piotr Hendzel, Piotr Zielenkiewicz and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 25 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Michał Konwerski1st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland.
Agnieszka GromadkaInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland.
Adam ArendarczykDepartment of Cardiac Surgery, Medical University of Warsaw, Warsaw, Poland.
Marta KoblowskaInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland.
Roksana Iwanicka-NowickaInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland.
Radosław WilimskiDepartment of Cardiac Surgery, Medical University of Warsaw, Warsaw, Poland.ORCID 0000-0002-3408-3997
Paweł CzubDepartment of Cardiac Surgery, Medical University of Warsaw, Warsaw, Poland.
Krzysztof Jerzy Filipiak1st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland.
Piotr HendzelDepartment of Cardiac Surgery, Medical University of Warsaw, Warsaw, Poland.
Piotr ZielenkiewiczInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland.ORCID 0000-0001-8151-6874
Grzegorz Opolski1st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland.ORCID 0000-0003-4744-2554
Aleksandra Gąsecka1st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland.ORCID 0000-0001-5083-7587
Tomasz Mazurek1st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland.
Medical University of Warsaw · PLInstitute of Biochemistry and Biophysics, Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePerivascular release of inflammatory mediators may accelerate coronary lesion formation and contribute to plaque instability. Accordingly, we compared gene expression in pericoronary adipose tissue (PCAT) in patients with advanced coronary artery disease (CAD) and non-CAD controls. PATIENTS AND

methodsPCAT samples were collected during coronary bypass grafting from CAD patients (n = 21) and controls undergoing valve replacement surgery, with CAD excluded by coronary angiography (n = 19). Gene expression was measured by GeneChip™ Human Transcriptome Array 2.0. Obtained list of 1348 transcripts (2.0%) that passed the filter criteria was further analyzed by Ingenuity Pathway Analysis software, identifying 735 unique differentially expressed genes (DEGs).

resultsAmong the CAD patients, 416 (30.9%) transcripts were upregulated, and 932 (69.1%) were downregulated, compared to controls. The top upregulated genes were involved in inflammation and atherosclerosis (chemokines, interleukin-6, selectin E and low-density lipoprotein cholesterol (LDL-C) receptor), whereas the downregulated genes were involved in cardiac ischaemia and remodelling, platelet function and mitochondrial function (miR-3671, miR-4524a, multimerin, biglycan, tissue factor pathway inhibitor (TFPI), glucuronidases, miR-548, collagen type I, III, IV). Among the top upstream regulators, we identified molecules that have proinflammatory and atherosclerotic features (High Mobility Group Box 2 (HMGB2), platelet-derived growth platelet (PDGF) and evolutionarily conserved signaling intermediate in Toll pathways (ESCIT)). The activated pathway related to DEGs consisted of molecules with well-established role in the pathogenesis of atherosclerosis (TFPI, plasminogen activator, plasminogen activator, urokinase receptor (PLAUR), thrombomodulin). Moreover, we showed that 22 of the altered genes form a pro-atherogenic network.

conclusionAltered gene expression in PCAT of CAD patients, with genes upregulation and activation of pathway involved in inflammation and atherosclerosis, may be involved in CAD development and progression.

Indexed as

adipose tissueatherosclerosisgene expressioninflammation

Identifiers

PMID34707383
PMCPMC8542577
OpenAlexW3207031644

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.